2017 Fiscal Year Final Research Report
Clarification of the mechanism of drug resistance focused on microRNAs associated with epithelial-mesenchymal transition in lung cancer
Project/Area Number |
15K19935
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Respiratory surgery
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Research Institution | Okayama University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 原発性肺癌 / 薬剤耐性機構 / マイクロRNA / 上皮間葉移行 |
Outline of Final Research Achievements |
It is a challenge to overcome the acquired resistance to EGFR tyrosine kinase inhibitors (EGFR-TKI) in lung cancers harboring EGFR activating mutations. Epithelial-mesenchymal transition (EMT), which was one of the mechanisms of the acquired resistance to EGFR-TKI, was associated with miR-200, one of microRNAs. In addition, the expression of LIN28B gene was elevated in EGFR-TKI-resistant lung cancer cell lines. Cell proliferation was inhibited by the induction of miR-200c or the knockdown of LIN28B in EGFR-TKI-resistant lung cancer cell lines. Thus, it is considered that LIN28B was a potential therapeutic target for lung cancer with the acquired resistance to EGFR-TKI.
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Free Research Field |
呼吸器外科学
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